ArticleProceedings of the National Academy of Sciences of the United States of America1996
The ATM homologue MEC1 is required for phosphorylation of replication protein A in yeast.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed.
- Article
- An Aurora B-RPA signaling axis secures chromosome segregation fidelity.Nature communications · 2023Article
- Comprehensive mutational analysis of the checkpoint signaling function of Rpa1/Ssb1 in fission yeast.PLoS genetics · 2023Article
- Recruitment of Scc2/4 to double-strand breaks depends on γH2A and DNA end resection.Life science alliance · 2022Article
- Review
- NSMF promotes the replication stress-induced DNA damage response for genome maintenance.Nucleic acids research · 2021Article
- Dynamic elements of replication protein A at the crossroads of DNA replication, recombination, and repair.Critical reviews in biochemistry and molecular biology · 2020Review
- A structural and dynamic model for the assembly of Replication Protein A on single-stranded DNA.Nature communications · 2018Article
- S-phase checkpoint regulations that preserve replication and chromosome integrity upon dNTP depletion.Cellular and molecular life sciences : CMLS · 2017Review
- The Dimeric Architecture of Checkpoint Kinases Mec1ATR and Tel1ATM Reveal a Common Structural Organization.The Journal of biological chemistry · 2016Article
- Managing Single-Stranded DNA during Replication Stress in Fission Yeast.Biomolecules · 2015Review
- Caffeine inhibits gene conversion by displacing Rad51 from ssDNA.Nucleic acids research · 2015Article
- Assembly of Slx4 signaling complexes behind DNA replication forks.The EMBO journal · 2015Article
- Phosphorylation of Sae2 Mediates Forkhead-associated (FHA) Domain-specific Interaction and Regulates Its DNA Repair Function.The Journal of biological chemistry · 2015Article
- Article
- Phosphorylation and cellular function of the human Rpa2 N-terminus in the budding yeast Saccharomyces cerevisiae.Experimental cell research · 2015Article
- Yeast PP4 interacts with ATR homolog Ddc2-Mec1 and regulates checkpoint signaling.Molecular cell · 2015Article
- Regulation of Elg1 activity by phosphorylation.Cell cycle (Georgetown, Tex.) · 2015Article
- Architecture and ssDNA interaction of the Timeless-Tipin-RPA complex.Nucleic acids research · 2014Article
- The C-terminal residues of Saccharomyces cerevisiae Mec1 are required for its localization, stability, and function.G3 (Bethesda, Md.) · 2013Article
33 more citing papers are in PubMed but not listed here.
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4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Replication protein A (RPA) is a highly conserved single-stranded DNA-binding protein, required for cellular DNA replication, repair, and recombination. In human cells, RPA is phosphorylated during the S and G2 phases of the cell cycle and also in response to ionizing or ultraviolet radiation. Saccharomyces cerevisiae exhibits a similar pattern of cell cycle-regulated RPA phosphorylation, and our studies indicate that the radiation-induced reactions occur in yeast as well. We have examined yeast RPA phosphorylation during the normal cell cycle and in response to environmental insult, and have demonstrated that the checkpoint gene MEC1 is required for the reaction under all conditions tested. Through examination of several checkpoint mutants, we have placed RPA phosphorylation in a novel pathway of the DNA damage response. MEC1 is similar in sequence to human ATM, the gene mutated in patients with ataxia-telangiectasia (A-T). A-T cells are deficient in multiple checkpoint pathways and are hypersensitive to killing by ionizing radiation. Because A-T cells exhibit a delay in ionizing radiation-induced RPA phosphorylation, our results indicate a functional similarity between MEC1 and ATM, and suggest that RPA phosphorylation is involved in a conserved eukaryotic DNA damage-response pathway defective in A-T.
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